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PubMed1977

[Ascorbic acid levels in the bronchopneumonia of calves].

The level of ascorbic acid in the blood plasma of 59 calves was determined. The age of the calves ranged between two and three months and the samples of blood were collected in January. The first group of calves included 30 animals displaying no clinical symptoms of disease: the average ascorbic acid level was 0.50 +/- 0.18 mg per 100 ml. In the second group, consisting of 19 calves, the blood of the animals was collected three weeks after the termination of the acute stage of bronchopneumonia; the average value of ascorbic acid was 0.30 +/- 0.14 mg per 100 ml. The lowest average value of ascorbic acid was obtained in the calves at an acute stage of bronchopneumonia, reaching 0.18 +/- 0.11 mg per 100 ml. The differences of results between groups I and II and between groups I and III were found to be statistically significant. A conspicuous drop of ascorbic acid level was ascertained in calves suffering from bronchopneumonia-this problem needs deeper scrutiny, owing to the fact that bronchopneumonia is responsible for considerable economic losses in large-capacity calf houses.

Acute Disease↗
PubMed1985

Biological nature of the effect of ascorbic acids on the growth of human leukemic cells.

The effects of L-ascorbic acid (LAA) on the in vitro growth of human leukemic colony-forming cells (L-CFC) were analyzed for all acute nonlymphocytic leukemia patients from whom bone marrow aspirates were received by this laboratory for cell culture study. Among 259 cases, 163 could be directly evaluated for LAA effect. L-CFC growth enhancement was noted in 53 (33%) and suppression in 28 (17%), with overall 50% of patients affected by LAA. Among 34 normal bone marrows tested, none were enhanced by LAA while 8 (24%) were suppressed. While caution is needed in interpreting L-CFC suppression by LAA, L-CFC enhancement is clearly significant. Two isomers of LAA, D-isoascorbic acid and D-ascorbic acid, which have weaker antiscorbutic activity than that of LAA, also produced the L-CFC growth-enhancing effect, but to a lesser degree than that of LAA. A dose-response study also substantiated that D-ascorbic acid was definitely less effective than was LAA. Since D-ascorbic acid is the true optical isomer of LAA and has identical physicochemical properties as does LAA, this differential effect is clearly of biological nature. This study indicates that L-CFC growth suppression by LAA is observed in one-sixth of leukemic patients, L-CFC enhancement in one-third of patients, and that L-CFC growth enhancement is a clearly significant finding with a biological mechanism as the basis.

Ascorbic Acid↗
PubMed2001

Microdialysis measurement of ascorbic acid in rabbit vitreous after photodynamic reaction.

A method for long-term intravitreous microdialysis was used to measure endogenous reduced ascorbic acid in the vitreous of rabbits by HPLC-ECD before and after exposure to intense visible light in the presence of fluorescein. Cellulose microdialysis probes were implanted into the vitreous humor of each eye and after stabilization ascorbic acid measurements were recorded over a 14 day period. Under this experimental condition, normal ascorbic acid concentrations in vitreous varied from 98.0 +/- 9.8 to 106.9 +/- 20.3 microM(mean +/- S.D.). The eyes received light irradiation (25 000 lux) for 2 hr and fluorescein was used as the photosensitizer once or twice. No immediate effects on ascorbic acid concentrations could be observed in the eyes irradiated twice without fluorescein i.v. injections and in the twice fluorescein injected without irradiation. However, in the eyes irradiated once with fluorescein (30 mg kg(-1)), ascorbic acid concentration after irradiation significantly decreased from day 2 and continued over a period of 10 days compared with that before irradiation and maximal reduction was 32.6% (P < 0.005) on day 6 after irradiation. By day 13, the ascorbic acid concentration returned to control levels (P > 0.01). In the eyes irradiated twice with fluorescein injections, ascorbic acid concentration after irradiation decreased even more over the experimental period and the maximal reduction was 65.5% (P < 0.005) on day 5 after irradiation and did not recover over the next 9 days. In the eyes irradiated twice with fluorescein injections plus administration of ascorbic acid (150 mg kg(-1)) 30 min before irradiation, a significant increase (52.5%) of ascorbic acid (P < 0.005) was found on day 1 and control levels of ascorbic acid were maintained from day 2 onward. The protective role of ascorbic acid in the vitreous humor against photodynamic reaction is suggested.

Animals↗
PubMed1998

Ascorbic acid deficiency changes hepatic gene expression of acute phase proteins in scurvy-prone ODS rats.

The ODS rat (genotype od/od), which has a hereditary defect in ascorbic acid biosynthesis, was used to investigate the effects of ascorbic acid deficiency on the hepatic gene expression of both the positive acute phase proteins, haptoglobin and alpha1-acid glycoprotein, and the negative acute phase proteins, apolipoprotein A-I and albumin. Male ODS rats (6 wk old, body weight approximately 140 g) were fed a basal diet containing ascorbic acid (300 mg/kg diet) or a diet without ascorbic acid for 14 d. Ascorbic acid deficiency significantly elevated the serum concentration of haptoglobin and significantly lowered those of apolipoprotein A-I and albumin. The hepatic mRNA levels of haptoglobin and alpha1-acid glycoprotein in the ascorbic acid-deficient rats were significantly elevated on d 12, and reached 260 (P < 0.05) and 360% (P < 0.01) of respective values in the control rats on d 14. On the contrary, the hepatic mRNA levels of apolipoprotein A-I and albumin in the ascorbic acid-deficient rats were lowered to 68 (P < 0.01) and 71% (P < 0.05) of respective values in the control rats on d 14. Although ascorbic acid deficiency significantly elevated the serum corticosterone concentration on d 14, the changes in mRNA levels of haptoglobin, alpha1-acid glycoprotein, apolipoprotein A-I and albumin due to ascorbic acid deficiency were not affected by adrenalectomy, as assessed in a separate experiment. The serum concentration of interleukin-6, an inflammatory cytokine that stimulates gene expression of some acute phase proteins, was significantly higher in the ascorbic acid-deficient rats on d 14 than in the control rats. These results suggest that ascorbic acid deficiency causes physiologic changes similar to those that occur in the acute phase response.

Acute-Phase Proteins↗
PubMed2002

Prolonged marginal ascorbic acid deficiency induces oxidative stress in retina of guinea pigs.

We examined whether prolonged marginal ascorbic acid deficiency induces oxidative stress in the retina of guinea pigs. Male guinea pigs aged four weeks were given a scorbutic diet (20 g/animal per day) with either marginally deficient ascorbic acid (0.5 mg/animal per day) or adequate ascorbic acid (1 g/animal per day) in drinking water for three and six months. The retinal contents of the reduced form of ascorbic acid in the deficient group at three and six months were 68.1 and 43.5%, respectively, of that in the corresponding adequate group. The retinal contents of the oxidized form of ascorbic acid in the deficient group at three and six months were 1.9- and 2.7-fold, respectively, higher than that in the corresponding adequate group. The content of retinal thiobarbituric acid reactive substances (TBARS), an index of lipid peroxidation, in the deficient group was 2.5-fold higher than that in the adequate group at six months. The retinal contents of reduced glutathione (GSH) in the deficient group at three and six months were 84.8 and 66.7%, respectively, of that in the corresponding adequate group. The deficient group had 37.5% of retinal vitamin E content of the adequate group at six months. The deficient group had higher serum vitamin E concentration than the adequate group in both experimental periods. There were no differences in serum TBARS and GSH concentrations between the groups at both periods. These results indicate that prolonged marginal ascorbic acid deficiency induces oxidative stress in the retina of guinea pigs without systemic oxidative stress.

Animals↗
PubMed1976

The hydrolytic activity of L-ascorbic acid.

The ability of L-ascorbic acid to catalyze the liberation of 4-methylumbelliferone from 4-methylumbelliferyl-beta-D-N-acetylglucosaminide, 4-methylumbelliferyl-beta-D-glucuronide, 4-methylumbelliferyl-alpha-D-mannoside, and 4-methylumbelliferyl-beta-D-galactoside is documented. There is an apparent metal and oxygen dependency. The cleavage of two lipids was shown in addition to the hydrolysis of these fluorogenic glycosides. Galactose was liberated from galactosyl-6-[3H]ceramide and oleic acid from cholesterol-[1-14C]oleate by L-ascorbic acid under conditins usually used for in vitro incubations. In common with most in vitro systems, only a small percentage of substrate was degraded.

Ascorbic Acid↗
PubMed1984

Effect of large intake of ascorbic acid on urinary and plasma oxalic acid levels.

Blood samples form ten healthy subjects, who had been ingesting 3-10 g of ascorbic acid for at least two years, were collected. The ascorbic acid and oxalic acid levels in the plasma of these subjects were measured. The concentrations of oxalic acid in these plasma samples are within the range of plasma oxalate levels of human subjects who were not ingesting ascorbic acid supplements. Large quantities of ascorbic acid (10 g/day) were administered to healthy human subjects. Daily urinary samples of these subjects were collected before and during treatment. Urinary ascorbic acid and oxalic acid levels of these samples were measured. Among the six subjects tested, five experienced no significant change on urinary oxalate excretion. Urinary oxalate level of one subject was significantly elevated upon the large intake of ascorbic acid. But the increased daily excretion of oxylate in this subject is within the changes in urinary oxalate content from consuming normal diets.

Adult↗
PubMed1987

Characteristics of the transport of ascorbic acid into leucocytes.

The degree and the mode of association of [14C]-ascorbic acid with leucocytes are examined. The degree of association of ascorbic acid with polymorphonuclear leucocytes (1-3%) is dependent on cell type, extracellular concentration of ascorbic acid, incubation temperature, intactness of the cells and the extracellular pH. All experiments are performed according to strict protocols as these compounds are labile in aqueous solutions. Further it is noticed that in all experiments an outward gradient of leucocyte endogenic ascorbic acid exists. The results suggest that the association process comprises at least one saturable pathway. The activation of polymorphonuclear leucocytes by phorbol myristate acetate increases the accumulation of ascorbic acid threefold.

Adult↗
PubMed1975

Apparent sulfation of glycosaminoglycans by ascorbic acid 2-[3 5-S] sulfate: an explanation.

The sulfation of glycosaminoglycans by ascorbic acid 2-[35S]sulfate was studied in costal cartilage and chondrocytes in vitro. Negligable (if any) sulfation of glycosaminoglycans was detected with immediately isolated ascorbic acid 2-[35S]sulfate. However, formation of [35S]glycosaminoglycans was readily detected with ascorbic acid 2-[35S]sulfate which had been stored at minus 20 degrees C for several days. The [35S]glycosaminoglycans did not result from the direct transfer of 35S from ascorbic acid 2-sulfate but rather from a decomposition product of ascorbic acid 2-[35S]sulfate. Evidence is presented to show that the sulfation pathway with the decomposition product involves exchange with inorganic sulfate, and strongly suggests that sulfation proceeds via 3'-phosphoadenosine 5'-phosphosulfate. The decomposition product appears similar to inorganic sulfate in several test systems. In view of these observations, it is suggested that previous conclusions implicating as acid 2-sulfate as a biological sulfate donor, based on the use of ascorbic acid 2-[35S]sulfate be re-evaluated.

Adenine Nucleotides↗
PubMed2002

The effect of ascorbic acid and L-histidine therapy on acute mammary inflammation in dairy cattle.

Ascorbic acid and L-histidine were investigated as antioxidant therapies for acute mammary inflammation. Mastitis was induced in eight nonpregnant Holstein cows by intramammary infusion of endotoxin. Treatments were administered in a 4 x 4 Latin square crossover design with 1-wk periods between challenges with endotoxin. Four individual treatments, control, ascorbic acid only, L-histidine only, and ascorbic acid plus L-histidine, were applied. Two doses of 25 g of ascorbic acid administered intravenously at 3- and 5-h postendotoxin challenge increased milk production recovery (9% higher, P < 0.02) and tended to reduce the extent of rumen stasis. Two doses of 25 g of L-histidine similarly administered decreased plasma antioxidant activities 5.5% (P < 0.05). However, ascorbic acid and L-histidine had no effects on rectal temperature, heart rate, respiratory rate, and dry matter intake. The data suggested that ascorbic acid provided some potential benefit for recovery from acute mammary inflammation in dairy cattle.

Acute Disease↗
PubMed2005

Intravenous iron preparations and ascorbic acid: effects on chelatable and bioavailable iron.

BACKGROUND: There is growing interest to use ascorbic acid as adjuvant therapy for patients with recombinant human erythropoietin-hyporesponsiveness (rHuEpo). Several clinical studies showed the beneficial effect of ascorbic acid treatment on hematologic parameters in rHuEpo-treated hemodialysis patients with elevated or even normal iron stores. However, whether ascorbic acid directly affects stability and cellular metabolism of intravenous iron preparations (IVI) is not well understood. METHODS: The preparations for testing were iron sucrose (Venofer), ferric gluconate (Ferrlecit), and iron dextran (INFeD). HepG2-cells were used to investigate effects of ascorbic acid on iron bioavailability for the intracellular labile iron pool (LIP) from IVI by using the fluorescent calcein-assay, and cellular ferritin content was measured by enzyme-linked immunosorbent assay (ELISA). Transferrin-chelatable iron was assessed by fluorescent-apotransferrin, and cell toxicity was assayed by neutral red cytotoxicity test. RESULTS: The effects of vitamin C on different preparations do not reflect their known chemical stability (i.e., iron dextran >iron sucrose >ferric gluconate). Effects of ascorbic acid on the increase of the intracellular LIP, as well as on increasing mobilization to transferrin in serum, were limited to iron sucrose. Ascorbic acid did not increase cell toxicity and the amount of low molecular weight iron in serum. CONCLUSION: We conclude that corrected ascorbic acid levels in hemodialysis (HD) patients could increase the amount of bioavailable iron from iron sucrose, but not from other classes of IVI. Vitamin C administration could therefore result in a lower need of iron sucrose to correct anemia.

Ascorbic Acid↗
PubMed1981

Effects of maternal intake of ascorbic acid on the postnatal metabolism of this vitamin in the guinea pig.

Guinea pigs were fed diets containing 0.04% (control), 0.56% (E-1) or 0.86% (E-2) ascorbic acid during the last half of pregnancy. Levels of ascorbic acid in serum and various organs of the mother and fetuses were higher in the animals receiving the E-1 diet than in controls. Between 5 and 10 days after birth ascorbic acid catabolism was measured in the offspring of the various groups by determining the rate of excretion of 14Co2 after an injection of L-[1-14C] ascorbic acid. Compared with controls, pups from the E-1 and E-2 groups had similar increased ascorbic acid catabolism. Animals in the E-1 group, fed a 0.006% (MDR) ascorbic acid diet from day 11 after birth, had markedly decreased ascorbic acid catabolism after ten days on the MDR diet. After 20 days on this diet ascorbic acid catabolism was similar to controls fed the MDR diet. By contrast, catabolism values remained elevated in pups maintained on the E-1 diet. Similarly, tissue ascorbic acid levels among all groups of offspring reflected comparable changes. Prolonged high maternal intake of ascorbic acid during pregnancy increases the metabolism of this vitamin in the neonatal period. Additional postnatal effects depend on dietary manipulation and may either be lasting or transient.

Animals↗
PubMed1997

[The in vitro effect of ascorbic acid on sodium nitrite intoxication].

The in vitro effect of ascorbic acid on the content of sodium nitrite in relation to pH and time of incubation and also effect of sodium nitrite on the total content of vitamin C as a sum of both reduced and oxidized forms was demonstrated. Ascorbic acid in respective quantities of 60 mg, 120 mg, 180 mg and sodium nitrite in quantity of 12 mg were added to the in vitro simulated stomach content at pH 1.5, 2.5, 3.5. The control samples were tested without addition of ascorbic acid. The Griess method for determination of nitrite and the Tillmans method with Pijanowski's modification were used for the determination of vitamin C. It was found that the choice of lower pH significantly decreased the level of nitrite in the control samples produced the disappearance of nitrite increased depending on the quantity of ascorbic acid added to the sample and on pH. The total content of vitamin C did not change after adding of sodium nitrite to the samples. The performed studies suggested a positive effect of ascorbic acid decreasing of the nitrite level.

Ascorbic Acid↗
PubMedDate not supplied

Stabilization of ascorbic acid and its measurement by liquid chromatography in nonfat dry milk.

The determination of ascorbic acid by liquid chromatography (LC) was improved by performing the analysis in the presence of solvents that had been purged with argon to reduce the concentration of oxygen. This methodological modification eliminated the oxidation of ascorbic acid during the chromatographic procedure and reduced the minimum detection level to 1 microgram. Solutions of ascorbic acid have been successfully stabilized for 67 days by addition of dithiothreitol to a deaerated solution of water-acetonitrile (25 + 75 v/v), sealed under argon in amber vials and stored at -20 degrees C. In a second independent study, a procedure for the extraction of ascorbic acid from nonfat dry milk in a single step was developed. The ascorbic acid content of Nonfat Dry Milk (SRM 1549) was determined by LC, using the method of standard additions. The mean ascorbic acid content was 54 +/- 5 micrograms/g of sample. Analysis of variance of the analytical results indicates that there is a significant continual increase in the content of the ascorbic acid in each bottle from first to last sample.

Animals↗
PubMed2001

Relation between plasma ascorbic acid and mortality in men and women in EPIC-Norfolk prospective study: a prospective population study. European Prospective Investigation into Cancer and Nutrition.

BACKGROUND: Ascorbic acid (vitamin C) might be protective for several chronic diseases. However, findings from prospective studies that relate ascorbic acid to cardiovascular disease or cancer are not consistent. We aimed to assess the relation between plasma ascorbic acid and subsequent mortality due to all causes, cardiovascular disease, ischaemic heart disease, and cancer. METHODS: We prospectively examined for 4 years the relation between plasma ascorbic acid concentrations and mortality due to all causes, and to cardiovascular disease, ischaemic heart disease, and cancer in 19 496 men and women aged 45-79 years. We recruited individuals by post using age-sex registers of general practices. Participants completed a health and lifestyle questionnaire and were examined at a clinic visit. They were followed-up for causes of death for about 4 years. Individuals were divided into sex-specific quintiles of plasma ascorbic acid. We used the Cox proportional hazard model to determine the effect of ascorbic acid and other risk factors on mortality. FINDINGS: Plasma ascorbic acid concentration was inversely related to mortality from all-causes, and from cardiovascular disease, and ischaemic heart disease in men and women. Risk of mortality in the top ascorbic acid quintile was about half the risk in the lowest quintile (p<0.0001). The relation with mortality was continuous through the whole distribution of ascorbic acid concentrations. 20 micromol/L rise in plasma ascorbic acid concentration, equivalent to about 50 g per day increase in fruit and vegetable intake, was associated with about a 20% reduction in risk of all-cause mortality (p<0.0001), independent of age, systolic blood pressure, blood cholesterol, cigarette smoking habit, diabetes, and supplement use. Ascorbic acid was inversely related to cancer mortality in men but not women. INTERPRETATION: Small increases in fruit and vegetable intake of about one serving daily has encouraging prospects for possible prevention of disease.

Age Distribution↗
PubMed1994

Dietary ascorbic acid lowers the concentration of soluble copper in the small intestinal lumen of rats.

We tested the hypothesis that ascorbic acid in the diet of rats lowers the concentration of soluble Cu in the small intestine, causing a decrease in apparent Cu absorption. Male rats were fed on diets adequate in Cu (5 mg Cu/kg) without or with 10 g ascorbic acid/kg. The diet with ascorbic acid was fed for either 6 or 42 d. Ascorbic acid depressed tissue Cu concentrations after a feeding period of 42, but not after 6 d. Dietary ascorbic acid lowered apparent Cu absorption after 6, but not after 42 d. The lowering of tissue Cu concentrations after long-term ascorbic acid feeding may have increased the efficiency of Cu absorption, and thus counteracted the inhibitory effect of ascorbic acid. Dietary ascorbic acid caused a significant decrease in the Cu concentrations in the liquid phase of both the proximal and distal parts of the small intestinal lumen. This effect was due to both a decrease in the amount of Cu in the liquid digesta and an increase in the volume of the liquid phase; only the latter effect for the distal intestine was statistically significant. We conclude that ascorbic acid supplementation lowers Cu absorption by decreasing the concentration of soluble Cu in the small intestine.

Animals↗
PubMed1989

Sex as a factor in levels of serum ascorbic acid in a healthy elderly population.

To investigate gender difference in serum ascorbic acid levels in healthy elderly, its status was studied in 175 free-living and healthy elderly people aged 63-81, who were not using ascorbic acid supplement. Both mean dietary ascorbic acid intake (3.2 +/- 1.3 mg/kg of body weight/day) and its serum concentration (1.11 +/- 0.23 mg/100 ml) for females (n = 96) were significantly higher than for males (2.7 +/- 1.1 mg/kg/day and 0.91 +/- 0.30 mg/100 ml; n = 79). It was estimated that intakes needed to maintain a serum ascorbic acid concentration of 1.0 mg/100 ml would be about 2 mg/kg of body weight/day for females and about 3 mg/kg/day for males. In this population, dietary ascorbic acid intake was the most important predictor of its serum concentration, but sex was also significantly related to it, accounting about 7% of its total variation.

Aged↗
PubMed1997

NADPH-initiated cytochrome P450-dependent free iron-independent microsomal lipid peroxidation: specific prevention by ascorbic acid.

In this paper we demonstrate that ascorbic acid specifically prevents NADPH-initiated cytochrome P450 (P450)-mediated microsomal lipid peroxidation in the absence of free iron. Lipid peroxidation has been evidenced by the formations of conjugated dienes, lipid hydroperoxide and malondialdehyde. Other scavengers of reactive oxygen species including superoxide dismutase, catalase, glutathione, alpha-tocopherol, uric acid, thiourea, mannitol, histidine, beta-carotene and probucol are ineffective to prevent the NADPH-initiated P450-mediated free iron-independent microsomal lipid peroxidation. Using a reconstituted system comprised of purified NADPH-P450 reductase, P450 and isolated microsomal lipid or pure L-alpha-phosphatidylcholine diarachidoyl, a mechanism has been proposed for the iron-independent microsomal lipid peroxidation and its prevention by ascorbic acid. It is proposed that the perferryl moiety P450 Fe3+.O2.- initiates lipid peroxidation by abstracting methylene hydrogen from polyunsaturated lipid to form lipid radical, which then combines with oxygen to produce the chain propagating peroxyl radical for subsequent formation of lipid peroxides. Apparently, ascorbic acid prevents initiation of lipid peroxidation by interacting with P450 Fe3+.O2.-.

Animals↗